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Department of Pathology, Tohoku University School of Medicine (T.S., H.S., G.H., J.T., Y.M., F.D., H.N.), and the Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University (S.S.), Sendai 980-8575, Japan; and the Laboratory of Molecular Hypertension, Baker Medical Research Institute (Z.S.K.), Melbourne, Australia
Address all correspondence and requests for reprints to: Takashi Suzuki M.D., Department of Pathology, Tohoku University School of Medicine, 2–1 Seiryo-machi, Aoba-ku, Sendai, 980-8575, Japan. E-mail: t-suzuki{at}patholo2.med.tohoku.ac.jp
11ß-Hydroxysteroid dehydrogenase type 2 (11ßHSD2) catalyzes the conversion of cortisol to biologically inactive cortisone and is thought to confer specificity on mineralocorticoid receptors (MR). Cortisol is a prerequisite for surfactant synthesis and fetal lung maturation. Recently, expression of 11ßHSD2 was demonstrated in human fetal lung, but its localization and possible biological roles remain unknown. Therefore, in this study, we examined immunohistochemical localization of 11ßHSD2, MR, and glucocorticoid receptor (GR) in nonpathological human lungs from fetus to adult (8 weeks gestation to 55 yr of age; n = 40) retrieved from pathology files. Both 11ßHSD2 and MR immunoreactivities were detected in airway epithelia, from bronchiole to trachea and in fetal and neonatal ciliated collecting duct cells of tracheal and bronchial glands, but were undetectable in alveoli. On the other hand, GR was detected in all cell types. These results indicate that 11ßHSD2 colocalizes with MR in human airway epithelia and suggest that 11ßHSD2 play an important role in pulmonary mineralocorticoid activity such as sodium and fluid transport.
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